Plasma soluble fibrin monomer complexes in nephrotic syndrome-with reference to hypoalbuminemia.

Iioka, Yukio; Kikuchi, Kazuyoshi; Tada, Hayato; Isogai, Sho; Urayama, Tsutomu

doi:10.1620/tjem.143.53

Cited by 5 publications

(2 citation statements)

References 5 publications

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“…Several mechanisms have been proposed to explain the association between hypoalbuminemia and plasma D-dimer, including hypoalbuminemia-induced hypercoagulability and thrombosis [22,23]. Data from Bang et al and Iioka Y et al showed negative correlations between serum albumin level and plasma D-dimer level in patients with nephrotic syndrome [24,25]. A similar result was obtained by Remuzziet al [26].…”

Section: Discussionsupporting

confidence: 53%

Determinants of Elevated D-Dimer Levels and Long-Term Outcome in Elderly Patients With End-Stage Heart Failure

Tian

Yang

Weng

et al. 2021

Preprint

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Background Previous studies have shown that heart failure is associated with hemostatic abnormalities and hypercoagulable state. Plasma D-dimer levels reflect both fibrin formation and degradation, and elevated D-dimer levels have been associated with poor prognosis in patients with heart failure. However, little is known about their roles in elderly patients with end-stage HF. In present study, we aimed to explore the clinical significance and determinants of plasma D-dimer in elderly patients with end-stage heart failure. Methods A total of 177 patients with heart failure at Beijing Geriatric Hospital from November 1, 2015 to December 30, 2018 were enrolled. All hospitalized patients were obtained D-dimer levels within the first 24 h following admission after obtaining informed consent. Primary endpoint was all-cause mortality. Results A total of 60 patients had elevated D-dimer levels. Blood urea nitrogen (β = 1.106, 95% CI: 1.029–1.190, p = 0.006), NYHA functional class (β = 2.179, 95% CI: 1.170–4.056, p = 0.014) and white blood cell counts (β = 1.188, 95% CI: 1.040–1.358, p = 0.011) were independent risk factors for elevated D-dimer in elderly patients with end-stage heart failure. Albumin (β = 0.803, 95% CI: 0.728–0.885, P ༜ 0.001) was negative risk factor for elevated D-dimer in elderly patients with end-stage heart failure. Elevated D-dimer level was independently associated with increased risk of long-term all-cause mortality (P = 0.048). Conclusions For elderly patients with end-stage heart failure, D-dimer levels were associated with white blood cell counts, blood urea nitrogen, albumin and NYHA functional class and elevated D-dimer level was independently associated with poor long-term outcome.

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Section: Discussionsupporting

confidence: 53%

Determinants of Elevated D-Dimer Levels and Long-Term Outcome in Elderly Patients With End-Stage Heart Failure

Tian

Yang

Weng

et al. 2021

Preprint

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“…creased circulating fibrin(ogen) fragments which are themselves inhibitory may act synergistically with albumin. Iioka et al (1984) described an inverse relationship between circulating concentrations of albumin and fibrin complexes in some nephrotic syndrome patients. The two findings may reflect unrelated expressions of the same disease, since albumin was only moderately decreased.…”

Section: Discussionmentioning

confidence: 99%

Albumin modulates lateral assembly of fibrin polymers: evidence of enhanced fine fibril formation and of unique synergism with fibrinogen

Galanakis¹,

Lane²,

Simon³

1987

Biochemistry

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We identified a new property of human albumin. It enhances formation of fine fibril (or leptofibril) structures during fibrin gelation, and by nephelometric and electron microscopic measurements, this property is independent of and synergistic with that of fibrinogen. We examined fibrin aggregation using physiologic temperatures and pH and albumin:fibrin concentration ratios below those at which the known accelerating effect on fibrin aggregation occurs. An albumin concentration dependent decrease in gel turbidity maxima was consistently demonstrable in buffers containing or lacking (2-5 mM) CaCl2. This decrease was shown to be induced by albumin preparations which had been exposed to 2 mM ethylene-diaminetetraacetate disodium salt (EDTA), dialyzed, and tested in EDTA-free buffer. A delay in the onset of aggregation was also shown in calcium-lacking buffers by use of either reaggregating fibrin or fibrinogen aggregated with low (0.01-0.05 unit/mL) thrombin concentrations. Rates of fibrin aggregation as well as those of fibrinopeptide release were not affected by albumin, and the decrease in gel absorbance was demonstrable when solubilized fibrin was reaggregated at all final fibrin concentrations (0.2-4 microM) examined. Computed from wavelength dependence turbidity measurements (1 microM fibrin, I = 0.20), albumin decreased the average mass:length ratio from 8.24 X 10(11) to 4.26 X 10(11) daltons/cm, or from that of an approximately six to a three protofibril-thick strand. It also decreased the mean fibril radius from 48.5 to 36.4 nm but had no effect on fibril density. Electron microscopic measurements of cross-sectional fibril widths, performed on sections of glutaraldehyde-fixed gels, disclosed differences between albumin-containing and control gels which were significant by chi 2 analysis (P greater than 0.001). Fibril groups of 7-20- and 21-40-nm width together comprised 77% of fibrils formed in the presence of albumin (n = 251) compared to 30% of controls (n = 309). Conversely, coarser fibrils of 41-60- and 61-97-nm width together comprised 23% of fibrils formed in the presence of albumin and 70% of controls. This albumin effect was demonstrable by use of different monomeric albumin preparations including defatted, undefatted (unexposed and exposed to 60 degrees C, 10 h), chromatographically [gel exclusion and (diethylaminoethyl)cellulose] pure, S-(carboxymethyl)albumin, and S-(N-ethylsuccinimidyl)albumin. Chromatographically isolated albumin oligomers lacked this property, suggesting that a specific site(s) on albumin was (were) required.(ABSTRACT TRUNCATED AT 400 WORDS)

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Effect of increasing serum albumin on plasma D-dimer, von Willebrand factor, and platelet aggregation in CAPD patients

Kim

Sook

Park

et al. 1999

American Journal of Kidney Diseases

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Plasma soluble fibrin monomer complexes in nephrotic syndrome-with reference to hypoalbuminemia.

Cited by 5 publications

References 5 publications

Determinants of Elevated D-Dimer Levels and Long-Term Outcome in Elderly Patients With End-Stage Heart Failure

Determinants of Elevated D-Dimer Levels and Long-Term Outcome in Elderly Patients With End-Stage Heart Failure

Albumin modulates lateral assembly of fibrin polymers: evidence of enhanced fine fibril formation and of unique synergism with fibrinogen

Effect of increasing serum albumin on plasma D-dimer, von Willebrand factor, and platelet aggregation in CAPD patients

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